Down syndrome is the most common chromosomal disorder compatible with life and is associated with multisystem manifestations, including visual abnormalities. Refractive errors are among the most frequent ocular manifestations in Down syndrome, occurring at substantially higher rates than in the general population. Unlike typically developing children, who largely achieve emmetropia through a homeostatic process called emmetropization, children with Down syndrome show a low proportion of emmetropia and persistently heterogeneous refractive errors. This integrative review searched PubMed/MEDLINE, Scopus, Google Scholar, and the Cochrane Library to synthesize evidence on three domains hypothesized to interact in producing emmetropization failure in Down syndrome: corneal biomechanical alteration, accommodative dysfunction, and disrupted retinal blur signalling. Available evidence suggests that trisomy 21 is associated with dysregulated extracellular matrix and collagen organization that reduces corneal biomechanical stability, together with accommodation lag markedly greater than in children without Down syndrome. Both mechanisms appear to converge on persistent retinal image degradation, which may disrupt the visual signals required for refractive growth regulation and contribute to persistent ametropia, increased amblyopia risk, and long-term impairment of visual development. An integrated understanding of these mechanisms has important implications for longitudinal ophthalmologic screening strategies, early amblyopia detection, and more routine evaluation of accommodative function in the Down syndrome population.
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